I went to the actual study, and this, I believe, is where it conclusively shows it's not only “potentiating:”
Next, we established a PDX from a patient who had been treated with cisplatin-based therapy but developed treatment resistance. This PDX was found to natively express a high level of TMEM16A. We treated mice bearing this PDX with either vehicle control or cisplatin with or without HCQ, skipping the HCQ alone group because of the abundance of data indicating HCQ as a safe drug in vitro as well as CAM experiments. HCQ treatment restored sensitivity to cisplatin in this PDX (Fig. 6C), suggesting that lysosomal inhibition potentiates cisplatin toxicity in vivo. To determine cellular damage inflicted through HCQ, we used phospho-histone H2AX, a marker for DNA double-strand break. Immunohistochemistry of PDX tissue stained with pH2AX shows significantly increased positively stained bodies in the combination group, further supporting our hypothesis that HCQ sensitizes the tumor tissue to cisplatin-induced death (Fig. 6D).
Yes, it does also potentiate it, as described further below, though.
Thoughts? I always appreciate your insight.
I commend you for your knowledge and thoroughness. If I read what you included it says that the HCQ alone trial was skipped. I wish they had done it to truly see if HCQ on its own was tumor lytic. I agree potentiation may be the wrong word but it sure does look like and excellent adjuvant to therapy.
The golden age of cancer treatment is upon us with -mab (monoclonal targeted) treatment and specific genetic therapy.
Thanks for positing all you do. You add a significant amount of knowledge to our forum.